Research article summary (published 29 Sep 2009):

Mycobacterial antigen-induced T helper type 1 (Th1) and Th2 reactivity of peripheral blood mononuclear cells from diabetic and non-diabetic tuberculosis patients and Mycobacterium bovis bacilli Calmette-Guérin (BCG)-vaccinated healthy subjects.

Full Abstract

Patients with diabetes mellitus are more susceptible to tuberculosis (TB), and the clinical conditions of diabetic TB patients deteriorate faster than non-diabetic TB patients, but the immunological basis for this phenomenon is not understood clearly. Given the role of cell-mediated immunity (CMI) in providing protection against TB, we investigated whether CMI responses in diabetic TB patients are compromised. Peripheral blood mononuclear cells (PBMC) obtained from diabetic TB patients, non-diabetic TB patients and Mycobacterium bovis bacilli Calmette-Guérin (BCG)-vaccinated healthy subjects were cultured in the presence of complex mycobacterial antigens and pools of M. tuberculosis regions of difference (RD)1, RD4, RD6 and RD10 peptides. The PBMC were assessed for antigen-induced cell proliferation and secretion of T helper 1 (Th1) [interferon (IFN)-gamma, interleukin (IL)-2, tumour necrosis factor (TNF)-beta], and Th2 (IL-4, IL-5, IL-10) cytokines as CMI parameters. All the complex mycobacterial antigens and RD1(pool) stimulated strong proliferation of PBMC of all groups, except moderate responses to RD1(pool) in healthy subjects. In response to complex mycobacterial antigens, both IFN-gamma and TNF-beta were secreted by PBMC of all groups whereas diabetic TB patients secreted IL-10 with concentrations higher than the other two groups. Furthermore, in response to RD peptides, IFN-gamma and IL-10 were secreted by PBMC of diabetic TB patients only. The analyses of data in relation to relative cytokine concentrations showed that diabetic TB patients had lower Th1 : Th2 cytokines ratios, and a higher Th2 bias. The results demonstrate a shift towards Th2 bias in diabetic TB patients which may explain, at least in part, a faster deterioration in their clinical conditions.

Author information

Author/s: Al-Attiyah, R J (RJ); Mustafa, A S (AS);

Affiliation: Department of Microbiology, Kuwait University, Safat, Kuwait. rj.alattiyah(-atsign-)hsc.edu.kw

Journal and publication information

Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

Journal: Clinical and experimental immunology (Clin Exp Immunol), published in England. (Language: eng)

Reference: 2009-Oct; vol 158 (issue 1) : pp 64-73

Dates: Created 2009/09/09; Completed 2009/10/09; Revised 2009/10/14;

PMID: 19737232, status: MEDLINE (last retrieval date: 10/15/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Adult Antigens, Bacterial - pharmacology BCG Vaccine Biological Markers - analysis Cell Proliferation - drug effects Cells, Cultured Diabetes Mellitus - immunology; microbiology Disease Susceptibility Female Flow Cytometry Humans Immunization

Interferon-gamma - analysis Interleukin-10 - analysis Interleukin-2 - analysis Lymphotoxin-alpha - analysis Male Middle Aged Mycobacterium bovis - immunology T-Lymphocytes - immunology Th1 Cells - immunology Th2 Cells - immunology Tuberculosis, Pulmonary - complications; immunology; prevention & control Young Adult

Associated Chemicals: Antigens, Bacterial (0) ; BCG Vaccine (0) ; Biological Markers (0) ; Interleukin-2 (0) ; Lymphotoxin-alpha (0) ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6)

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